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γ‐Aminobutyric acid type B receptor changes in the rat striatum and substantia nigra following intrastriatal quinolinic acid lesions
Author(s) -
Rekik Letaïef,
DaguinNerrière Véronique,
Petit JeanYves,
Brachet Philippe
Publication year - 2011
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22574
Subject(s) - quinolinic acid , striatum , substantia nigra , glial fibrillary acidic protein , pars compacta , medicine , endocrinology , gabaa receptor , receptor , chemistry , biology , biochemistry , amino acid , immunohistochemistry , dopaminergic , dopamine , tryptophan
Changes in the regional distribution of the metabotropic GABA type B receptors (GABA B ) were investigated in a rat model of Huntignton's disease. Animals received a unilateral intrastriatal injection of quinolinic acid (QA), and GABA B immunoreactivity was monitored 3, 11, and 21 days postinjection in the striatum and substantia nigra (SN). Two antibodies, recognizing either the GABA B1 or the GABA B2 receptor subtypes, were used. QA injection rapidly induced a protracted increase in GABA B1 or GABA B2 immunoreactivity in the lesioned striatum, despite the neuronal loss. In the SN, a continuous increase in GABA B1 and GABA B2 immunoreactivity was observed at all time points in the ipsilateral pars reticulata (SNr), whereas the pars compacta (SNc) was unaffected by this phenomenon. This increase was supported by a densitometric analysis. At day 21 postlesion induction, intensely labeled stellate cells and processes were found in the ipsilateral SNr, in addition to immunoreactive neurons. Double labeling of GABA B1 and glial fibrillary acidic protein (GFAP) showed that the stellate cells were reactive astrocytes. Hence, part of the sustained increase in GABA B immunoreactivity that takes place in the SNr and possibly the striatum may be ascribed to reactive astrocytes. It is suggested that GABA B receptors are up‐regulated in these reactive astrocytes and that agonists might influence the extent of this astroglial reaction. © 2011 Wiley‐Liss, Inc.